Background Whether intraoperative use of hydroxyethyl starch impairs kidney function remains unknown. The authors thus tested the primary hypothesis that Hextend promotes renal injury in surgical patients. Secondarily, the authors evaluated the dose–outcome relationship, in-hospital and 90-day mortality, and whether the relationship between colloid use and acute kidney injury (AKI) depends on baseline risk for AKI. Methods The authors evaluated the data of 44,176 adults without preexisting kidney failure who had inpatient noncardiac surgery from 2005 to 2012. Patients given a combination of colloid and crystalloid were propensity matched on morphometric, and baseline characteristics to patients given only crystalloid. The primary analysis was a proportional odds logistic regression with AKI as an ordinal outcome based on the Acute Kidney Injury Network classification. Results The authors matched 14,680 patients receiving colloids with 14,680 patients receiving noncolloids for a total of 29,360 patients. After controlling for potential confounding variables, the odds of developing a more serious level of AKI with Hextend was 21% (6 to 38%) greater than with crystalloid only (P = 0.001). AKI risk increased as a function of colloid volume (P < 0.001). In contrast, the relationship between colloid use and AKI did not differ on baseline AKI risk (P = 0.84). There was no association between colloid use and risk of in-hospital (P = 0.81) or 90-day (P = 0.02) mortality. Conclusion Dose-dependent renal toxicity associated with Hextend in patients having noncardiac surgery is consistent with randomized trials in critical care patients.
Background Glucose-insulin-potassium (GIK) administration during cardiac surgery inconsistently improves myocardial function, perhaps because hyperglycemia negates the beneficial effects of GIK. The hyperinsulinemic normoglycemic clamp (HNC) technique may better enhance the myocardial benefits of GIK. We extended previous GIK investigations by: 1) targeting normoglycemia while administering a glucose-insulin-potassium infusion (HNC); 2) using improved echocardiographic measures of myocardial deformation, specifically myocardial longitudinal strain and strain rate; and, 3) assessing activation of glucose metabolic pathways. Methods 100 patients having aortic valve replacement for aortic stenosis were randomly assigned to HNC (high-dose insulin with concomitant glucose infusion titrated to normoglycemia) versus standard therapy (insulin treatment if glucose >150 mg/dL). Our primary outcomes were left ventricular longitudinal strain and strain rate, assessed using speckle-tracking echocardiography. Right atrial tissue was analyzed for activation of glycolysis/pyruvate oxidation and alternative metabolic pathways. Results Time-weighted mean glucose concentrations were lower with HNC (127±19 mg/dL) than standard care (177±41 mg/dL; P<0.001). Echocardiographic data were adequate in 72 patients for strain analysis and 67 patients for strain rate analysis. HNC did not improve myocardial strain, with an HNC minus standard therapy difference of −1.2 (97.5%CI: −2.9, 0.5)%; P=0.11. Strain rate was significantly better, but by a clinically unimportant amount: −0.16 (−0.30, −0.03) sec−1, P = 0.007. There was no evidence of increased glycolytic, pyruvate oxidation, or hexosamine biosynthetic pathway activation in right atrial samples (n = 20, HNC; 22, standard therapy). Conclusions Administration of glucose and insulin while targeting normoglycemia during aortic valve replacement did not meaningfully improve myocardial function.
Background The immediate effect of aortic valve replacement (AVR) for aortic stenosis on perioperative myocardial function is unclear. Left ventricular (LV) function may be impaired by cardioplegia-induced myocardial arrest and ischemia-reperfusion injury, especially in patients with LV hypertrophy. Alternatively, LV function may improve when afterload is reduced following AVR. The right ventricle (RV), however, experiences cardioplegic arrest without benefiting from improved loading conditions. Which of these effects on myocardial function dominate in patients undergoing AVR for aortic stenosis has not been thoroughly explored. Our primary objective thus to characterize the effect of intraoperative events on LV function during AVR using echocardiographic measures of myocardial deformation. Secondarily, we evaluated RV function. Methods In this supplementary analysis of 100 patients enrolled in a clinical trial (NCT01187329), 97 patients underwent AVR for aortic stenosis. Of these patients, 95 had a standardized intraoperative transesophageal echocardiographic examination of systolic and diastolic function performed before surgical incision and repeated after chest closure. Echocardiographic images were analyzed off-line for global longitudinal myocardial strain and strain rate using 2-dimensional speckle-tracking echocardiography. Myocardial deformation assessed at the beginning of surgery was compared with the end of surgery using paired t-tests corrected for multiple comparisons. Results LV volumes and arterial blood pressure decreased, and heart rate increased at the end of surgery. Echocardiographic images were acceptable for analysis in 72 patients for LV strain, 67 for LV strain rate, and 54 for RV strain and strain rate. In 72 patients with LV strain images, 9 patients required epinephrine, 22 required norepinephrine, and 2 required both at the end of surgery. LV strain did not change at the end of surgery compared with the beginning of surgery [difference: 0.7 (97.6%CI: 0.2, 1.5)%; P =0.07] while LV systolic strain rate improved (became more negative) [−0.3 (−0.4, −0.2) sec−1; P<0.001]. In contrast, RV systolic strain worsened (became less negative) at the end of surgery [difference: 4.6 (3.1, 6.0)%; P< 0.001] although RV systolic strain rate was unchanged [0.0 (97.6% CI: −0.1, 0.1); P = 0.83]. Conclusion LV function improved after replacement of a stenotic aortic valve demonstrated by improved longitudinal strain rate. In contrast, RV function, assessed by longitudinal strain, was reduced.
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